Granulosa cells obtained from estrogen-primed, hypophysectomized, immature female rats (HIFR) do not bind significant amounts of PRL. However, FSH treatments in vivo have been shown to induce detectable PRL receptors in the granulosa cells, an effect that is accentuated by injecting bGH in addition to oFSH. HIFR granulosa cells have been shown to synthesize and secrete prostaglandin E and F-2 alpha in vitro in amounts that are determined by the hormonal state of the animals from which they are excised. Pretreatment with injections of oFSH causes prostaglandin synthesis to increase in a dose-responsive fashion. Addition of bGH to the injection schedule has little effect on the oFSH-induced prostaglandin synthesis when 50 to 100 microgram oFSH doses x 3 are injected but acts to suppress the synthesis of prostaglandin when the 200 microgram oFSH dosage schedule has been employed. Addition of prolactin to the in vitro incubations of the cells from oFSH-treated animals causes a suppression of both PGE and PGF-2 alpha synthesis. Prolactin appears to suppress prostaglandin synthesis in the ovary as bGH may affect the ovary by making it more susceptible to the effects of PRL. Whether modification of the prostaglandin cascade is the mechanism of action of prolactin or whether it is just an incidental result of the PRL effect remains to be determined.